Valvular heart disease Flashcards
Incompetence of a valve stemming form an abnormality in one of its support structures, as opposed to a primary valve defect
Functional regurgitation
General secondary change from valvular stenosis
Pressure overload cardiac hypertrophy
General secondary change from mitral or aortic valvular insufficiency
Volume overload
Etiologies of abnormalities of leaflets and commissures leading to mitral regurgitation
Post-inflammatory scarring
Infective endocarditis
Mitral valve prolapse
Drugs (fen-phen)
Etiologies of abnormalities in tensor apparatus leading to mitral regurgitation
Rupture of papillary muscle
Papillary muscle dysfunction (fibrosis)
Rupture of chordae tendinae
Etiologies of abnormalities of LV and/or annulus leading to mitral regurgitation
LV enlargement –> myocarditis or dilated cardiomyopathy
Calcification of mitral ring
Etiology of mitral stenosis
Post inflammatory scarring –> rheumatic heart disease
Etiologies of aortic stenosis
Post inflammatory scarring –. rheumatic heart disease
Senile calcification
Calcification of congenitally deformed valve
Etiologies of aortic regurgitation
Post inflammatory scarring –> rheumatic heart disease
Degenerative aortic dilation
Syphilitic aortitis
Ankylosing spondylitis
RA
Marfan syndrome
Typical criteria for critical aortic stenosis
Area is <0.8 cm^2
Normal aortic valve area
3.5-4.0 cm^2
Age where symptoms typically present in congenital aortic stenosis
50 yr
Pathology of congenital aortic stenosis
Bicuspid valve
Foci of dystrophic calcification on aortic valves
Degenerative aortic stenosis
Consequences over time in aortic stenosis
Reduced compliance of LV
Significant increased in LVEDP
Hypertrophy of LA
Change in diastolic PV curve in aortic stenosis
Moves upward
Change in isovolumic pressure curve in aortic stenosis
Upward and leftward
Reason for angina in aortic stenosis
Increased myocardial oxygen demand and reduced oxygen supply
Symptoms that may occur in aortic stenosis
Angina
Syncope on exertion
HF
Reason for exertional syncope in aortic stenosis
Peripheral vasodilation and inability to augment CO results in decreased cerebral perfusion pressure
Changes in carotid pulse in aortic stenosis
Weakened/parvus and delated/tardus upstroke
Reason for carotid pulse changes in aortic stenosis
Fixed, obstructed LV flow
Murmur of aortic stenosis
Crescendo-decrescendo systolic ejection murmur heard best at base that often radiates to neck and apex
Reason for S4 heart sounds in aortic stenosis
Due to atrial contraction into the stiff LV
Compensation of aortic regurgitation
Eccentric hypertrophy
Combination of high LV SV and high systolic arterial pressure with a reduced aortic diastolic pressure. Widened pulse pressure.
Aortic regurgitation
Symptoms of acute aortic regurgitation
Dyspnea and pulmonary edema
Change in PV loop in aortic regurgitation
Diastolic PV curve shifts right
Isovolumic PV curve shifts left at first, then right
Very large SV
Change in pulse in aortic regurgitation
Hyperdynamic pulses due to widened pulse pressures
Types of hyperdynamic pulses
Water hammer/Corrigan
Quincke
DeMusset sign
Muller sign
DeMusset sign
Head-bobbing from widened pulse pressure
Muller sign
Rhythmic pulsation of the uvula due to widened pulse pressure
Quincke pulse
Arterial pulsation seen in nail bed
Water hammer or Corrigan pulse
Sudden rise then drop in pressure
High-pitched, blowing, early diastolic murmur heard best along the L sternal border.
Aortic regurgitation
Normal mitral valve area
5-6 cm^2
Mitral valve area when hemodynamic changes become apparent
<2 cm^2
Cause of dyspnea in mitral stensois
Transudation of plasma into lung interstitium and alveoli because of increased pressure
Cause of hemoptysis in mitral stenosis
Collateral between bronchial and pulmonary veins leading to engorgement and rupture of bronchial V
Complication of chronic pressure overload in LA in mitral stenosis
A fib –> intra-mural thombus
PV loop changes in mitral stenosis
Decreased SV
Overall slight shift left
Symptom of mild mitral stenosis
Dyspnea on exertion
Symptoms of severe mitral stenosis
Dyspnea at rest
Increasing fatigue
Orthopnea
PND
Cause of hoarseness of voice related to mitral stenosis
Enlarged pulmonary A or LA compresses the recurrent laryngeal N
Ortner syndrome
Hoarseness due to compression of recurrent laryngeal N from enlarged cardiovascular structures
High pitches opening snap after S2. Followed by a low-frequency decrescendo diastolic murmur
Mitral stenosis
Best indicator of mitral stenosis severity on auscultation
A2-OS interval shortens as LA pressure increases
Antibodies in rheumatic fever
To streptolysin O and DNase B
JONES criteria of rheumatic fever
Joint pain –> migratory polyarthritis
Carditis
Nodules in skin, subcutaneous
Erythema marginatum
Sydenham’s chorea
Hypersensitivity in transient migratory polyarthritis in rheumatic fever
Type II hypersensitivity –> results from formation of immune complexes
Cross-reaction of antibodies in rheumatic fever
To group A carbohydrate or streptococcal M protein
Affect of IgG antibodies on valve endothelium in rheumatic fever
Upregulate vascular cell adhesion 1 (VCAM1) and promote infiltration of T cells
Aschoff nodule formation in acute rheumatic fever
Result of intense inflammatory process, mainly mediated by CD4 cells. Form on valves
Pathological consequences of inflammation from acute rheumatic fever on the heart
Dilation of valve annuli
Elongation of chordae tendinae
Rings that surround heart valve that help close leaflets during systole
Valve annuli
Foci of T cells, occasional plasma cells, and plump activated macrophages seen microscopically in acute rheumatic fever
Aschoff bodies
Anitschkow cells
Plump activated macrophages
Anatomic changes of the mitral valve in rheumatic heart disease
Leaflet thickening
Commissural fusion and shortening
Thickening and fusion of tendinous cords
Results in stenosis
Compensation in mitral regurgitation
LA and LV dilation and hypertrophy
PV loop changes in mitral regurgitation
Diastolic shifts rightward
Significantly increased SV
Isovolemic eventually shifts R
Cardiac marker changes in acute mitral regurgitation
Significantly increased preload
Decreased afterload
No change in contractile function
Significantly increased EF
Decreased forward SV
Cardiac marker changes in compensated chronic mitral regurgitation
Increased preload
No change in afterload, contractility, or forward SV
Increased EF
Cardiac marker changes in decompensated mitral regurgitation
Increased preload and afterload
Decreased contractility, EF, and forward SV
Best indicator of mitral regurgitation severity
Audible S3
Irregular, stony, hard, and occasionally ulcerated nodules at the base of the mitral valve leaflets
Mitral annular calcification
Possible complication of mitral annular calcification
Embolic stroke
Infective endocarditis
Mitral valve disorder associated with heritable CT disorders and excess TGF-beta activity
Mitral valve prolapse
Mid-systolic click that may be followed by a mid to late systolic murmur best heard at apex
Mitral valve prolapse
Rare serious complications of mitral valve prolapse
Infective endocarditis
Mitral insufficiency, possibly with chordal rupture
Stroke or other systemic infarct
Arrhythmias
Affected mitral leaflets are often enlarged, redundant, thick, and rubbery. Tendinous cords may be elongated, thinned, or ruptured, Annulus may be dilated.
Mitral valve prolapse
Microscopy of mitral valve shows marked thickening of the spongiosa layer with deposition of mucoid/myxomatous material. Attenuation of collagenous fibrosa layer of the valve.
Mitral valve prolapse
Stain that makes collagen yellow, elastin black, and proteoglycans blue.
Movat pentachrome stain
Microbial infection of the heart valves or mural endocardium leading to formation of vegetations composed of thrombotic debris and organisms.
Infective endocarditis
Modified duke criteria of infective endocarditis
Fever
Roth spots
Osler nodes
Murmur
Janeway lesions
Anemia
Nail bed splinter hemorrhages
Emboli
White-centered retinal hemorrhages
Roth spots
Painful, red, raised lesions on the hands and feet. Associated with infective endocarditis.
Osler nodes
Irregular, nontender, hemorrhagic macules located on the palms and soles. Associated with infective endocarditis
Janeway lesions
Complications of infective endocarditis
Glomerulonephritis
Septic arterial or pulmonary emboli
Friable, bulky, potentially destructive lesions containing fibrin, inflammatory cells, and infectious organism that form vegetations on heart valves.
Infective endocarditis
Form when infectious vegetations erode into the underlying myocardium and produce an abscess in infective endocarditis
Ring abscess
Deposition of small, bland, sterile thrombi on the leaflets of cardiac valves. Non-invasive and do not elicit inflammatory reaction.
Nonbacterial thrombotic endocarditis
Marantic endocarditis
Nonbacterial thrombotic endocarditis in pts with cancer or sepsis
Conditions associated with nonbacterial thrombotic endocarditis
DVT
PE
Hypercoagulable states
Endocardial trauma
Condition associated with Libman-Sacks endocarditis
SLE
Pink, sterile vegetations on undersurface of AV valves with a warty/verrucous appearance
Libman-Sacks endocarditis
Complication of Libman-Sacks endocarditis
Mitral and tricuspid valvulitis
Complications of transcatheter aortic valve replacement (TAVR)
Paravalvular lead
Stroke
MI
Reason for MI post TAVR
Obstruction of coronary A ostia by implanted valve
Reason for paravalvular leak in TAVR
Inappropriate size or position of valve
Improper sealing to native annulus
Blood leakage around valve
Aortic regurgitation